The Effect of Iodinated Contrast Agent Properties on Renal Kinetics and Oxygenation

Abstract

We identified a superior profile for the low-osmolar CAs compared with the iso-osmolar CAs regarding rapid excretion, short-term renal exposure, and renal oxygenation.

Limb ischemic preconditioning protects against contrast-induced acute kidney injury in rats via phosphorylation of GSK-3β

“…The protective effect of LIPC on ischemia/reperfusion injury has been shown to be associated with activation of the reperfusion injury salvage kinases (RISK) pathway, in which PI3K/Akt and ERK1/2 signaling leads to the phosphorylation of glycogen synthase kinase-3β (GSK-3β) [10,11]. In addition, several studies [12][13][14] have shown that hypoperfusion and hypoxia in the renal medulla occur within minutes after the injection of CM, and the kidney then suffers from subsequent reperfusion injury and reactive oxygen species (ROS) generation. We hypothesized that the RISK signaling pathway is involved in the renoprotection induced by LIPC.…”

Atherosclerotic renal artery stenosis is associated with elevated cell cycle arrest markers related to reduced renal blood flow and postcontrast hypoxia

“…It can be affected by variations in R2 (= 1/T2) because, for example, of changes in water content [48]. Although the second BOLD MRI was done 24 h after contrast administration, we cannot exclude the possibility that contrast retention within the kidney could affect R2 [49]. Studies of water loading in normal volunteers demonstrated a change in cortical R2 of 0.72/s, while R2* fell by 1.36/s.…”

Comparison of the Effects of Iodixanol and Iopamidol on Urine Flow, Urine Viscosity, and Glomerular Filtration in Rats

“…Here, the difference in CM osmolalities plays a major role (290 versus 796 mosmol/kg H 2 O) [29,32,41]. Non-reabsorbable CM diminish the osmotic gradient that drives tubular water resorption, thereby inducing osmodiuresis.…”

“…Please note that the very high creatinine clearance values for the first sampling period following CM (0-10 min, depicted as grey shadows) do not represent actual increases in glomerular filtration rate, but rely on the dead-space effect (see Results). [2,20,28,29,[32][33][34][35]. Hypoxia is part of a vicious circle that entails cellular damage, oxidative stress and vasoconstriction [2,28,29].…”

“…Studies in rats and minipigs showed that the higher urine viscosity leads to a longer renal retention of IOCM than LOCM [32,35,41,43], which is accompanied by higher levels of injury markers [32,41]. Also, intrarenal oxygenation was much more compromised following IOCM than LOCM as monitored by invasive probes and blood oxygenation leveldependent (BOLD) magnetic resonance [20,32,33,35].…”